Bottom Line:
These effects were pronounced in patients who were beta-blocker naïve (32% of all patients with CHF).These effects were pronounced in patients who were beta-blocker naïve.The underlying mechanism remains to be elucidated.

Background: Overproduction of pro-inflammatory cytokines is a well established factor in the progression of chronic heart failure (CHF). Changes in cellular immunity have not been widely studied, and the impact of standard medication is uncertain. Here we investigate whether a leukocyte redistribution occurs in CHF and whether this effect is influenced by beta-blocker therapy.

Principal findings: While no differences in the number of leukocytes were noted between patients with CHF and healthy controls, we detected relative lymphopenia in patients with CHF (p<0.001 vs. control), mostly driven by reductions in T helper cells and B cells (both p<0.05). The number of neutrophils was increased (p<0.01). These effects were pronounced in patients who were beta-blocker naïve (32% of all patients with CHF). Increased plasma levels of soluble tumor necrosis receptor-1 correlated with the relative number of lymphocyte subsets.

Conclusions: In patients with CHF, we detected a redistribution of leukocyte subsets, i.e. an increase in neutrophils with relative lymphopenia. These effects were pronounced in patients who were beta-blocker naïve. The underlying mechanism remains to be elucidated.

Mentions:
Whole blood from both healthy subjects and patients with CHF produced substantial levels of TNFα and IL-6 when stimulated with 0.1, 1, 10, or 100 ng/mL LPS (Figure 1). There was a trend towards higher LPS-stimulated TNFα production levels in patients with CHF than in healthy control subjects at two LPS concentrations, 0.1 (p = 0.05) and 1 ng/mL (p = 0.06). There was no significant difference with regards to the serum concentrations of C-reactive protein, IL-1β, and TNFα (all p>0.25, Table 2). There were significantly higher levels of IL-6 (p<0.0001), soluble TNFα receptor (sTNFR) 1 (p = 0.0025), and sTNFR-2 (p = 0.0007, Table 2).

Bottom Line:
These effects were pronounced in patients who were beta-blocker naïve (32% of all patients with CHF).These effects were pronounced in patients who were beta-blocker naïve.The underlying mechanism remains to be elucidated.

Background: Overproduction of pro-inflammatory cytokines is a well established factor in the progression of chronic heart failure (CHF). Changes in cellular immunity have not been widely studied, and the impact of standard medication is uncertain. Here we investigate whether a leukocyte redistribution occurs in CHF and whether this effect is influenced by beta-blocker therapy.

Principal findings: While no differences in the number of leukocytes were noted between patients with CHF and healthy controls, we detected relative lymphopenia in patients with CHF (p<0.001 vs. control), mostly driven by reductions in T helper cells and B cells (both p<0.05). The number of neutrophils was increased (p<0.01). These effects were pronounced in patients who were beta-blocker naïve (32% of all patients with CHF). Increased plasma levels of soluble tumor necrosis receptor-1 correlated with the relative number of lymphocyte subsets.

Conclusions: In patients with CHF, we detected a redistribution of leukocyte subsets, i.e. an increase in neutrophils with relative lymphopenia. These effects were pronounced in patients who were beta-blocker naïve. The underlying mechanism remains to be elucidated.